Kaitlin Day, RMIT University and Sharayah Carter, RMIT University

Intermittent fasting has gained popularity in recent years as a dietary approach with potential health benefits. So you might have been surprised to see headlines last week suggesting the practice could increase a person’s risk of death from heart disease.

The news stories were based on recent research which found a link between time-restricted eating, a form of intermittent fasting, and an increased risk of death from cardiovascular disease, or heart disease.

So what can we make of these findings? And how do they measure up with what else we know about intermittent fasting and heart disease?

The study in question

The research was presented as a scientific poster at an American Heart Association conference last week. The full study hasn’t yet been published in a peer-reviewed journal.

The researchers used data from the National Health and Nutrition Examination Survey (NHANES), a long-running survey that collects information from a large number of people in the United States.

This type of research, known as observational research, involves analysing large groups of people to identify relationships between lifestyle factors and disease. The study covered a 15-year period.

It showed people who ate their meals within an eight-hour window faced a 91% increased risk of dying from heart disease compared to those spreading their meals over 12 to 16 hours. When we look more closely at the data, it suggests 7.5% of those who ate within eight hours died from heart disease during the study, compared to 3.6% of those who ate across 12 to 16 hours.

We don’t know if the authors controlled for other factors that can influence health, such as body weight, medication use or diet quality. It’s likely some of these questions will be answered once the full details of the study are published.

It’s also worth noting that participants may have eaten during a shorter window for a range of reasons – not necessarily because they were intentionally following a time-restricted diet. For example, they may have had a poor appetite due to illness, which could have also influenced the results.

Other research

Although this research may have a number of limitations, its findings aren’t entirely unique. They align with several other published studies using the NHANES data set.

For example, one study showed eating over a longer period of time reduced the risk of death from heart disease by 64% in people with heart failure.

Another study in people with diabetes showed those who ate more frequently had a lower risk of death from heart disease.

A recent study found an overnight fast shorter than ten hours and longer than 14 hours increased the risk dying from of heart disease. This suggests too short a fast could also be a problem.

But I thought intermittent fasting was healthy?

There are conflicting results about intermittent fasting in the scientific literature, partly due to the different types of intermittent fasting.

There’s time restricted eating, which limits eating to a period of time each day, and which the current study looks at. There are also different patterns of fast and feed days, such as the well-known 5:2 diet, where on fast days people generally consume about 25% of their energy needs, while on feed days there is no restriction on food intake.

Despite these different fasting patterns, systematic reviews of randomised controlled trials (RCTs) consistently demonstrate benefits for intermittent fasting in terms of weight loss and heart disease risk factors (for example, blood pressure and cholesterol levels).

RCTs indicate intermittent fasting yields comparable improvements in these areas to other dietary interventions, such as daily moderate energy restriction.

So why do we see such different results?

RCTs directly compare two conditions, such as intermittent fasting versus daily energy restriction, and control for a range of factors that could affect outcomes. So they offer insights into causal relationships we can’t get through observational studies alone.

However, they often focus on specific groups and short-term outcomes. On average, these studies follow participants for around 12 months, leaving long-term effects unknown.

While observational research provides valuable insights into population-level trends over longer periods, it relies on self-reporting and cannot demonstrate cause and effect.

Relying on people to accurately report their own eating habits is tricky, as they may have difficulty remembering what and when they ate. This is a long-standing issue in observational studies and makes relying only on these types of studies to help us understand the relationship between diet and disease challenging.

It’s likely the relationship between eating timing and health is more complex than simply eating more or less regularly. Our bodies are controlled by a group of internal clocks (our circadian rhythm), and when our behaviour doesn’t align with these clocks, such as when we eat at unusual times, our bodies can have trouble managing this.

So, is intermittent fasting safe?

There’s no simple answer to this question. RCTs have shown it appears a safe option for weight loss in the short term.

However, people in the NHANES dataset who eat within a limited period of the day appear to be at higher risk of dying from heart disease. Of course, many other factors could be causing them to eat in this way, and influence the results.

When faced with conflicting data, it’s generally agreed among scientists that RCTs provide a higher level of evidence. There are too many unknowns to accept the conclusions of an epidemiological study like this one without asking questions. Unsurprisingly, it has been subject to criticism.

That said, to gain a better understanding of the long-term safety of intermittent fasting, we need to be able follow up individuals in these RCTs over five or ten years.

In the meantime, if you’re interested in trying intermittent fasting, you should speak to a health professional first.

Kaitlin Day, Lecturer in Human Nutrition, RMIT University and Sharayah Carter, Lecturer Nutrition and Dietetics, RMIT University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Mitochondria are tiny structures in cells that convert the food we eat into the energy our cells need to function.

Mitochondrial disease (or mito for short) is a group of conditions that affect this ability to generate the energy organs require to work properly. There are many different forms of mito and depending on the form, it can disrupt one or more organs and can cause organ failure.

There is no cure for mito. But an IVF procedure called mitochondrial donation now offers hope to families affected by some forms of mito that they can have genetically related children free from mito.

After a law to allow mitochondrial donation in Australia was passed in 2022, scientists are now preparing for a clinical trial to see if mitochondrial donation is safe and works.

What is mitochondrial disease?

There are two types of mitochondrial disease.

One is caused by faulty genes in the nuclear DNA, the DNA we inherit from both our parents and which makes us who we are.

The other is caused by faulty genes in the mitochondria’s own DNA. Mito caused by faulty mitochondrial DNA is passed down through the mother. But the risk of disease is unpredictable, so a mother who is only mildly affected can have a child who develops serious disease symptoms.

Mitochondrial disease is the most common inherited metabolic condition affecting one in 5,000 people.

Some people have mild symptoms that progress slowly, while others have severe symptoms that progress rapidly. Mito can affect any organ, but organs that need a lot of energy such as brain, muscle and heart are more often affected than other organs.

Mito that manifests in childhood often involves multiple organs, progresses rapidly, and has poor outcomes. Of all babies born each year in Australia, around 60 will develop life-threatening mitochondrial disease.

What is mitochondrial donation?

Mitochondrial donation is an experimental IVF-based technique that offers people who carry faulty mitochondrial DNA the potential to have genetically related children without passing on the faulty DNA.

It involves removing the nuclear DNA from the egg of someone who carries faulty mitochondrial DNA and inserting it into a healthy egg donated by someone not affected by mito, which has had its nuclear DNA removed.

The resulting egg has the nuclear DNA of the intending parent and functioning mitochondria from the donor. Sperm is then added and this allows the transmission of both intending parents’ nuclear DNA to the child.

A child born after mitochondrial donation will have genetic material from the three parties involved: nuclear DNA from the intending parents and mitochondrial DNA from the egg donor. As a result the child will likely have a reduced risk of mito, or no risk at all.

This highly technical procedure requires specially trained scientists and sophisticated equipment. It also requires both the person with mito and the egg donor to have hormone injections to stimulate the ovaries to produce multiple eggs. The eggs are then retrieved in an ultrasound-guided surgical procedure.

Mitochondrial donation has been pioneered in the United Kingdom where a handful of babies have been born as a result. To date there have been no reports about whether they are free of mito.

Maeve’s Law

After three years of public consultation The Mitochondrial Donation Law Reform (Maeve’s Law) Bill 2021 was passed in the Australian Senate in 2022, making mitochondrial donation legal in a research and clinical trial setting.

Maeve’s law stipulates strict conditions including that clinics need a special licence to perform mitochondrial donation.

To make sure mitochondrial donation works and is safe before it’s introduced into Australian clinical practice, the law also specifies that initial licences will be issued for pre-clinical and clinical trial research and training.

We’re expecting one such licence to be issued for the mitoHOPE (Healthy Outcomes Pilot and Evaluation) program, which we are part of, to perfect the technique and conduct a clinical trial to make sure mitochondrial donation is safe and effective.

Before starting the trial, a preclinical research and training program will ensure embryologists are trained in “real-life” clinical conditions and existing mitochondrial donation techniques are refined and improved. To do this, many human eggs are needed.

The need for donor eggs

One of the challenges with mitochondrial donation is sourcing eggs. For the preclinical research and training program, frozen eggs can be used, but for the clinical trial “fresh” eggs will be needed.

One possible source of frozen eggs is from people who have stored eggs they don’t intend to use.

A recent study looked at data on the outcomes of eggs stored at a Melbourne clinic from 2012 to 2021. Over the ten-year period, 1,132 eggs from 128 patients were discarded. No eggs were donated to research because the clinics where the eggs were stored did not conduct research requiring donor eggs.

However, research shows that among people with stored eggs, the number one choice for what to do with eggs they don’t need is to donate them to research.

This offers hope that, given the opportunity, those who have eggs stored that they don’t intend to use might be willing to donate them to mitochondrial donation preclinical research.

As for the “fresh” eggs needed in the future clinical trial, this will require individuals to volunteer to have their ovaries stimulated and eggs retrieved to give those people impacted by mito a chance to have a healthy baby. Egg donors may be people who are friends or relatives of those who enter the trial, or it might be people who don’t know someone affected by mito but would like to help them conceive.

At this stage, the aim is to begin enrolling participants in the clinical trial in the next 12 to 18 months. However this may change depending on when the required licences and ethics approvals are granted.

Karin Hammarberg, Senior Research Fellow, Global and Women’s Health, School of Public Health & Preventive Medicine, Monash University; Catherine Mills, Professor of Bioethics, Monash University; Mary Herbert, Professor, Anatomy & Developmental Biology, Monash University, and Molly Johnston, Research fellow, Monash Bioethics Centre, Monash University

This article is republished from The Conversation under a Creative Commons license. Read the original article.